Macronutrient preference, dietary intake, and substrate oxidation among stable cirrhotic patients

Citation
Him. Davidson et al., Macronutrient preference, dietary intake, and substrate oxidation among stable cirrhotic patients, HEPATOLOGY, 29(5), 1999, pp. 1380-1386
Citations number
53
Categorie Soggetti
Gastroenerology and Hepatology","da verificare
Journal title
HEPATOLOGY
ISSN journal
02709139 → ACNP
Volume
29
Issue
5
Year of publication
1999
Pages
1380 - 1386
Database
ISI
SICI code
0270-9139(199905)29:5<1380:MPDIAS>2.0.ZU;2-K
Abstract
Anorexia in liver disease is common; however, its association with aberrant metabolism and the type of cirrhosis has not been considered, Dietary inta ke, nutritional status, fasting substrate oxidation, and macronutrient pref erence were examined in controls (n = 18) and 65 patients with hepatocellul ar (n = 31) or biliary cirrhosis (n = 34). Energy intakes were lowest in he patocellular patients (controls: 9.0 +/- 0.48 megajoules/day compared with biliary: 7.0 +/- 0.40 MJ/day P < .05; controls compared with hepatocellular 6.5 +/- 0.39 megajoules/day, P < .01), Triceps skinfold was lower only in hepatocellular patients (controls: 109 +/- 9.2% compared with hepatocellula r 79 +/- 5.6%, P < .05), The fasting rate of lipid oxidation was elevated i n hepatocellular patients when compared with controls and biliary patients (controls: 40.9 +/- 15.1 mg/min compared with hepatocellular 62.8 +/- 16.8 mg/min, P < .001, and biliary : 45.5 +/- 17.0 mg/min compared with hepatoce llular, P < .001), Control subjects exhibited a greater preference for the high fat, moderate carbohydrate food (controls: median 7.0 IQR 2.0 compared with biliary: median 5.0 interquartile range [IQR] 4.7, P < .01) (controls compared with hepatocellular: median 6.0 IQR 4.0, P < .01), Cirrhotic pati ents' spontaneous dietary intake is lower than that of controls and recomme nded intakes. Although macronutrient preference ratings were different with in cirrhotic patient groups it remains unclear whether associated nutrient deficits are metabolically driven and dictated by primary cause.